Orientation Processing Deficits in Amblyopia: Neural Bases to Functional Implications

弱视的定向处理缺陷：神经基础到功能意义

基本信息

批准号：
10649039
负责人：
Qasim Zaidi
金额：
$ 24.53万
依托单位：
STATE COLLEGE OF OPTOMETRY
依托单位国家：
美国
项目类别：
财政年份：
2023
资助国家：
美国
起止时间：
2023-06-01 至 2025-05-31
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10649039
关键词：
3-Dimensional Adult Affect Algorithms Amblyopia Anisometropia Area Blindness Brain Calibration Cataract Cells Child Classification Compensation Computer Models Cues Darkness Data Detection Development Dimensions Disabled Persons Disease Electrophysiology (science)Eye Frequencies Future Health Human Image Learning Letters Life Link Macular degeneration Maps Methods Modeling Neurons Ocular Dominance Ocular dominance columns Optics Output Pattern Perception Perceptual distortions Performance Physiological Population Process Psychophysics Recovery Research Research Personnel Resolution Role Sampling Shapes Signal Transduction Stimulus Strabismus Sum System Testing Time Training V1 neuron Variant Vision Visual Visual Acuity Visual Cortex Visual Pathways area striata base cell cortex cortex mapping deprivation design experimental study improved model development monocular neural neural model neurodevelopment orientation selectivity parallel processing response retinal imaging spatial vision visual stimulus

项目摘要

PROJECT SUMMARY Amblyopia is a disorder of spatial vision despite good retinal image quality and eye health. It affects 2-3% of the population and almost always develops with early misalignment (strabismus) or unequal refractive power (anisometropia), or form deprivation (cataract). Most studies on human amblyopia concentrate on thresholds for contrast, size or offset, but striking perceptual distortions have been documented by asking amblyopes to describe or draw clearly visible high-contrast letters, rings, and sinusoidal gratings. Form distortions are likely to be at least as big a problem as loss of visual resolution for daily life. Forms are defined by local orientations, and almost all neurons in primary visual cortex (V1) are tuned for orientation, highlighting its importance in parsing visual images. The replicable systematic perceptual distortions of gratings drawn by amblyopes are unexplainable with a neural scrambling model or a systematic shift in the neural map, but are compatible with errors in the neural encoding of orientation in V1, while also involving decoding mechanisms in later cortical areas. Our team of researchers and clinicians proposes to examine the neural development and functional implications of the grating distortions by using our recent psychophysics, electrophysiology and modeling results in the domains of ON/OFF system imbalance in amblyopia, cortical map formation, orientation processing across V1, and the processing of parallel orientation signals for perceptions of 3-D shape, object pose and mirror symmetry. We aim to model the neural development of errors in orientation encoding as a consequence of ON-OFF imbalance caused by anisometropia and strabismus, which limits the orientation tuning and spatial resolution of V1 neurons and shrinks the ocular dominance columns for the amblyopic eye. We will also examine if orientation processing errors in the amblyopic eye make it difficult to do higher level tasks that rely on orientation cues, or if there is some compensatory mechanism, and if the fellow eye performs normally, overcompensates, or is handicapped because the lack of stereo makes it difficult to calibrate monocular cues during development. Psychophysical and electrophysiological data suggest that amblyopia also involves abnormalities in cortical areas after V1, suggesting that physiological changes may be propagated and amplified in higher cortical areas that may have prolonged windows of plasticity. In addition, regions of V1 that are unresponsive during passive viewing of visual stimuli in macular degeneration, can be activated by engaging the subjects in a stimulus-related task, suggesting a role for top-down influences on plasticity. The stimuli we use to identify deficits in functionally important visual tasks could be used to trigger top-down signals from higher brain areas as part of the design of future treatments for recovery of perceptual performance in adulthood, which would supplement treatments for improving visual acuity and binocularity. Possibly the biggest payoff could come from directly testing if top-down signals from these tasks reactivate plasticity in orientation selective V1 neurons in adult amblyopes.

项目概要尽管视网膜图像质量和眼睛健康良好，但弱视是一种空间视觉障碍。影响2-3% 人群中几乎总是出现早期错位（斜视）或屈光力不等（屈光参差）或形觉剥夺（白内障）。大多数关于人类弱视的研究都集中在阈值上对于对比度、大小或偏移，但通过要求弱视患者描述或绘制清晰可见的高对比度字母、环和正弦光栅。可能会出现形式扭曲至少与日常生活中视觉分辨率的丧失一样大。形式是由局部方向定义的，初级视觉皮层 (V1) 中的几乎所有神经元都针对方向进行了调整，凸显了其在解析视觉图像。弱视者绘制的光栅的可复制系统感知扭曲是无法用神经置乱模型或神经图谱的系统性转变来解释，但与 V1 方向的神经编码错误，同时还涉及后期皮质的解码机制地区。我们的研究人员和临床医生团队建议检查神经发育和功能通过使用我们最近的心理物理学、电生理学和建模来研究光栅畸变的影响导致弱视、皮质图形成、定向等领域的开/关系统不平衡 V1 上的处理，以及用于感知 3D 形状、物体的平行方向信号的处理姿势和镜像对称。我们的目标是将方向编码错误的神经发展建模为屈光参差和斜视引起的开关不平衡的结果，限制了方向 V1 神经元的调谐和空间分辨率，并缩小弱视眼的眼优势列。我们还将检查弱视眼的定向处理错误是否会导致难以达到更高水平依赖方向线索的任务，或者是否存在某种补偿机制，以及另一只眼睛是否执行通常，补偿过度，或者由于缺乏立体声而难以校准发育过程中的单眼线索。心理物理学和电生理学数据表明弱视还涉及 V1 后皮质区域的异常，表明生理变化可能是在可能具有延长可塑性窗口的较高皮质区域中传播和放大。此外，黄斑变性患者被动观看视觉刺激时无反应的 V1 区域通过让受试者参与与刺激相关的任务来激活，这表明自上而下的影响作用可塑性。我们用来识别功能上重要的视觉任务缺陷的刺激可以用来触发来自高级大脑区域的自上而下的信号，作为未来感知恢复治疗设计的一部分成年后的表现，这将补充改善视力和双眼视力的治疗。最大的回报可能来自直接测试这些任务的自上而下的信号是否重新激活成人弱视患者定向选择性 V1 神经元的可塑性。